INITIAL EVALUATION OF THE PATIENT WITH POISONING OR

DRUG OVERDOSE

Patients with drug overdoses or poisoning may initially present with no symptoms or with varying degrees of overt intoxication. The asymptomatic patient may have been exposed to or may have ingested a lethal dose of a poison but not yet have any manifestations of toxicity. It is always important to

• (1) quickly assess the potential danger

• (2) perform gut decontamination to prevent absorption, and

• (3) observe the patient for an appropriate interval.

Assess the Danger

• If the toxin is known, the danger can be assessed by consulting a text or computerized information resource (eg, POISINDEX) or by calling a regional poison control center

• Assessment will usually take into account the dose ingested (in milligrams per kilogram of body weight), the time interval since ingestion, the presence of any clinical signs, preexisting cardiac, respiratory, renal, or liver disease, and, occasionally, specific serum drug or toxin levels. Be aware that the history given by the patient or family may be incomplete or unreliable.

Observation of the Patient

• Asymptomatic or mildly symptomatic patients should be observed for at least 4–6 hours. Longer observation is indicated if the ingested substance is a sustained-release preparation or is known to slow gastrointestinal motility or if there may have been exposure to a poison with delayed onset of symptoms (such as acetaminophen, colchicine, or hepatotoxic mushrooms). After that time, the patient may be discharged if no symptoms have developed and adequate gastric decontamination has been provided. Before discharge, psychiatric evaluation should be performed to assess suicidal risk. Intentional ingestions in adolescents should raise the possibility of unwanted pregnancy or sexual abuse.

THE SYMPTOMATIC PATIENT

• COMA

• Assessment & Complications

• Coma is commonly associated with ingestion of large doses of antihistamines, barbiturates, benzodiazepines, ethanol, opioids, phenothiazines, or tricyclic antidepressants

• The most common cause of death in comatose patients is respiratory failure, which may occur abruptly. Aspiration of gastric contents may also occur, especially in victims who are deeply obtunded or convulsing. Hypoxia and hypoventilation may cause or aggravate arrhythmias and seizures. Thus, protection of the airway and assisted ventilation are the most important treatment measures for any poisoned patient.

Treatment

• A. Emergency Management: The initial emergency management of coma can be remembered by the mnemonic ABCD,for Airway, Breathing, Circulation, and Drugs (dextrose, thiamine, and naloxone or flumazenil)

Airway

• Establish a patent airway by positioning, suction, or insertion of an artificial nasal or oropharyngeal airway. If the patient is deeply comatose or if there is no gag or cough reflex, perform endotracheal intubation. These airway interventions may not be necessary if the patient is intoxicated by an opioid or a benzodiazepine and responds rapidly to intravenous naloxone or flumazenil

Breathing

• Clinically assess the quality and depth of respiration, and provide assistance if necessary with a bag-valve-mask device or mechanical ventilator. Provide supplemental oxygen. The arterial blood CO2 tension is useful in determining the adequacy of ventilation. The arterial blood PO2 determination may reveal hypoxemia, which may be caused by respiratory arrest, bronchospasm, pulmonary aspiration, or noncardiogenic pulmonary edema. Pulse oximetry is not reliable in patients with methemoglobinemia or carbon monoxide poisoning.

Circulation

• Measure the pulse and blood pressure, and estimate tissue perfusion (eg, by measurement of urinary output, skin signs, arterial blood pH). Insert an intravenous line, and draw blood for complete blood count, glucose, electrolytes, serum creatinine and liver tests, and possible toxicologic testing.

Drugs

• Dextrose and thiamine–Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50% dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.

Drugs

• Dextrose and thiamine–Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50% dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.

Drugs

• Dextrose and thiamine–Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50% dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.

Drugs

• Dextrose and thiamine–Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50% dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.

Drugs

• Dextrose and thiamine–Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50% dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.

Drugs

• Dextrose and thiamine–Unless promptly treated, severe hypoglycemia can cause irreversible brain damage. Therefore, in all comatose or convulsing patients, give 50% dextrose, 50–100 mL by intravenous bolus, unless a rapid bedside blood sugar test is available and rules out hypoglycemia. In alcoholic or very malnourished patients who may have marginal thiamine stores, give thiamine, 100 mg intramuscularly or over 2–3 minutes intravenously.

• Narcotic antagonists–Naloxone, 0.4–2 mg intravenously, may reverse opioid-induced respiratory depression and coma. If opioid overdose is strongly suspected, give additional doses of naloxone (up to 5–10 mg may be required to reverse potent opioids). Caution: Naloxone has a much shorter duration of action (2–3 hours) than most common opioids; repeated doses may be required, and continuous observation for at least 3–4 hours after the last dose is mandatory

• Flumazenil–Flumazenil, 0.2–0.5 mg intravenously, repeated every 30 seconds as needed up to a maximum of 3 mg, may reverse benzodiazepine-induced coma. Caution: Flumazenil has a short duration of effect (2–3 hours), and resedation requiring additional doses is common. Furthermore, flumazenil should not be given if the patient has co-ingested a tricyclic antidepressant or has a seizure disorder.

HYPOTHERMIA

• Assessment & Complications• Hypothermia commonly accompanies coma due to

opioids, ethanol, hypoglycemic agents, phenothiazines, barbiturates, benzodiazepines, and other sedative-hypnotics and depressants. Hypothermic patients may have a barely perceptible pulse and blood pressure and often appear to be dead. Hypothermia may cause or aggravate hypotension, which will not reverse until the temperature is normalized

HYPOTENSION

• Assessment & Complications• Hypotension may be due to poisoning by many

different drugs and poisons. The most common drugs causing hypotension are antihypertensive drugs, beta-blockers, calcium channel blocking agents, iron, theophylline, phenothiazines, barbiturates, and tricyclic antidepressants.

• Poisons causing hypotension include cyanide, carbon monoxide, hydrogen sulfide, arsenic, and certain mushrooms.

Treatment

• Most patients respond to empiric treatment (200 mL intravenous boluses of 0.9% saline or other isotonic crystalloid up to total of 1–2 L). If fluid therapy is not successful, give dopamine, 5–15 mg/kg/min by intravenous infusion in a large peripheral or central line. Consider pulmonary artery catheterization if hypotension persists.

• Hypotension caused by certain toxins may respond to specific treatment. For hypotension caused by overdoses of tricyclic antidepressants or related drugs, administer sodium bicarbonate, 1–2 meq/kg by intravenous bolus injection. For beta-blocker overdose, glucagon intravenously may be of value. For calcium antagonist overdose, administer calcium chloride, 15–20 mg/kg intravenously (repeated doses may be necessary).

HYPERTENSION

• Assessment & Complications

• Hypertension may be due to poisoning with amphetamines, anticholinergics, cocaine, phenylpropanolamine, or monoamine oxidase inhibitors (mainly as a result of a concomitantly administered drug).

• Severe hypertension (eg, diastolic blood pressure > 105–110 mm Hg in a person who does not have chronic hypertension) can result in acute intracranial hemorrhage, myocardial infarction, or aortic dissection. Patients often present with headache, chest pain, or encephalopathy

Treatment

• Treat hypertension (see Chapter 11) if the patient is symptomatic or if the diastolic pressure is greater than 105–110 mm Hg—especially if there is no prior history of hypertension.

• Administer phentolamine, 2–5 mg intravenously, or nitroprusside sodium, 0.25–8 mg/kg/min intravenously. If excessive tachycardia is present, add propranolol, 1–5 mg intravenously, or esmolol 25–100 mg/kg/min intravenously. Caution: Do not give beta-blockers alone, since doing so may paradoxically worsen hypertension.

ARRHYTHMIAS

• Assessment & Complications• Arrhythmias may occur with a variety of

drugs or toxins• They may also occur as a result of hypoxia,

metabolic acidosis, or electrolyte imbalance (eg, hyper- or hypokalemia, hypocalcemia), or following exposure to chlorinated solvents or chloral hydrate overdose.

Common toxins or drugs causing arrhythmias.

Arrhythmia• Sinus bradycardia

Common Causes• Beta-blockers,

verapamil, organophosphates, digitalis glycosides,

opioids, clonidine, sedative-hypnotics.

• Atrioventricular block

• Sinus tachycardia

• Wide QRS complex

• Beta-blockers, digitalis glycosides, calcium antagonists, tricyclic antidepressants, lithium.

• Theophylline, caffeine, cocaine, amphetamines, phencyclidine, beta-agonists (eg, albuterol), iron, anticholinergics, tricyclicantidepressants, antihistamines

• Tricyclic antidepressants, quinidine and class 1a antiarrhythmics,class 1c anti-arrhythmics, phenothiazines, potassium (hyperkalemia).

Treatment

• Arrhythmias are often caused by hypoxia or electrolyte imbalance, and these conditions should be sought and treated. If ventricular arrhythmias persist, administer lidocaine at usual antiarrhythmic doses. Caution: Avoid class Ia agents (quinidine, procainamide, disopyramide), which may aggravate arrhythmias caused by tricyclic antidepressants, calcium antagonists, or beta-blockers.Wide QRS complex tachycardia in the setting of tricyclic antidepressant overdose (or quinidine and other class Ia drugs) should be treated with sodium bicarbonate, 50–100 meq intravenously by bolus injection. For tachyarrhythmias induced by chlorinated solvents, chloral hydrate, or sympathomimetic agents, use propranolol or esmolol.

CONVULSIONS

• Assessment & Complications• Convulsions may be due to poisoning with many

drugs and poisons, including amphetamines, antihistamines, camphor, cocaine, isoniazid, lindane, phencyclidine (PCP), phenothiazines,, theophylline, and tricyclic antidepressants.

• Convulsions may also be caused by hypoxia, hypoglycemia, hypocalcemia, hyponatremia, withdrawal from alcohol or sedative-hypnotics, head trauma, central nervous system infection, or idiopathic epilepsy

Treatment

• Administer diazepam, 5–10 mg intravenously over 2–3 minutes, or lorazepam, 2–3 mg intravenously, or—if intravenous access is not immediately available—midazolam, 5–10 mg intramuscularly. If convulsions continue, administer phenobarbital, 15–20 mg/kg slowly intravenously over no less than 30 minutes; or phenytoin, 15 mg/kg intravenously over no less than 30 minutes (maximum infusion rate, 50 mg/min). The drugs may be used together if necessary

HYPERTHERMIA

• Assessment & Complications• Hyperthermia may be associated with poisoning by

amphetamines, atropine and other anticholinergic drugs, cocaine, dinitrophenol and pentachlorophenol, phencyclidine (PCP), salicylates, strychnine, tricyclic antidepressants, and various other medications

• Hyperthermia is a rapidly life-threatening complication. Severe hyperthermia (temperature > 40–41 °C) may rapidly cause brain damage and multiorgan failure, including rhabdomyolysis, renal failure, and coagulopathy

Treatment

• Treat hyperthermia aggressively by removing all clothing, spraying with tepid water, and fanning the patient. If this is not rapidly effective, as shown by a normal rectal temperature within 30–60 minutes, or if there is significant muscle rigidity or hyperactivity, induce neuromuscular paralysis with pancuronium, 0.1 mg/kg intravenously, or another nondepolarizing neuromuscular blocker

DECONTAMINATION OF THE SKIN

• Corrosive agents rapidly injure the skin and eyes and must be removed immediately. In addition, many toxins are readily absorbed through the skin, and systemic absorption can be prevented only by rapid action.

• Wash the affected areas with copious quantities of lukewarm water or saline. Wash carefully behind the ears, under the nails, and in skin folds. For oily substances (eg, pesticides), wash the skin at least twice with plain soap and shampoo the hair. Specific decontaminating solutions or solvents (eg, alcohol) are rarely indicated and in some cases may enhance absorption.

DECONTAMINATION OF THE EYES

• Act quickly to prevent serious damage. Flush the eyes with copious amounts of saline (preferred) or water. (If available, instill local anesthetic drops in the eye before beginning irrigation.) Remove contact lenses if present. Direct the irrigating stream so that it will flow across both eyes after running off the nasal bridge. Lift the tarsal conjunctiva to look for undissolved particles and to facilitate irrigation. Continue irrigation for 15 minutes by the clock or until each eye has been irrigated with at least 1 L of solution. If the toxin is an acid or a base, check the pH of the tears after irrigation, and continue irrigation until the pH is between 6.5 and 7.5.

GASTROINTESTINAL DECONTAMINATION

• Removal of ingested poisons is an essential part of emergency treatment. However, studies indicate that if more than 60 minutes has passed, induced emesis and gastric lavage are relatively ineffective

• For small or moderate ingestions of most substances, toxicologists generally recommend activated charcoal alone without prior gastric emptying. Exceptions are large ingestions of anticholinergic compounds and salicylates, which often delay gastric emptying, and ingestion of sustained-release or enteric-coated tablets, which may remain intact for several hours.

• Gastric emptying is not generally used for ingestion of corrosive agents or petroleum distillates, because further esophageal injury or pulmonary aspiration may result. However, in certain cases, removal of the toxin may be more important than concern over possible complications. Consult a medical toxicologist or regional poison control center for advices.

Emesis

• Emesis using syrup of ipecac is a convenient and fairly effective way to evacuate gastric contents if given very soon after ingestion (eg, at work or at home). However, it may delay or prevent use of oral activated charcoal and is not generally used in the hospital management of ingestions

• A. Indications: For removal of poison in conscious, cooperative patients and for promptness, ipecac can be given in the home or at work in the first few minutes after poisoning.

• B. Contraindications: Induced emesis is contraindicated for drowsy, unconscious, or convulsing patients and for patients who have ingested kerosene or other hydrocarbons (danger of aspiration of stomach contents), corrosive poisons, or rapidly acting convulsants (eg, tricyclic antidepressants, strychnine, nicotine, camphor).

• C. Technique: Give syrup of ipecac, 30 mL (15 mL in children), followed by an 8-oz glass of water. Repeat in 20 minutes if necessary

Gastric Lavage

• Gastric lavage is more effective for liquid poisons or small pill fragments than for intact tablets or pieces of mushroom. It is most effective when started within 60 minutes after ingestion. The lavage procedure may delay administration of activated charcoal and may hasten passage of pills and other toxic material into the small intestine.

Indications

• Gastric lavage is indicated for removal of ingested poisons when emesis is refused, contraindicated, or unsuccessful; for collection and examination of gastric contents for identification of poison; and for convenient administration of charcoal and antidotes.

Contraindications

• Do not use lavage for stuporous or comatose patients with absent gag reflexes unless they are endotracheally intubated beforehand. Some authorities advise against lavage when caustic material has been ingested; others regard it as essential to remove liquid corrosives from the stomach.

Technique

• In obtunded or comatose patients, the danger of aspiration pneumonia is reduced by placing the patient in a head down, left lateral decubitus position and, if necessary, protecting the airway with endotracheal intubation. Gently insert a lubricated, soft but noncollapsible stomach tube (at least 37–40F) through the mouth or nose into the stomach. Aspirate and save the contents, and then lavage repeatedly with 50–100 mL of fluid until the return fluid is clear. Use lukewarm tap water or saline

Activated Charcoal

• Activated charcoal effectively adsorbs almost all drugs and poisons. Poorly absorbed substances include iron, lithium, potassium, sodium, cyanide, mineral acids, and alcohols.

Indications

• Activated charcoal should be used for prompt adsorption of drugs or toxins in the stomach and intestine. Studies show that activated charcoal given alone may be as effective as or more effective than ipecac-induced emesis or gastric lavage.

Contraindications

• Activated charcoal should not be used for stuporous, comatose, or convulsing patients unless it can be given by gastric tube and the airway is first protected by cuffed endotracheal tube. This substance is contraindicated also for patients with ileus or intestinal obstruction or those who have ingested corrosives for whom endoscopy is planned.

Technique

• Administer activated charcoal, 60–100 g orally or via gastric tube, mixed in aqueous slurry. Repeated doses may be given to ensure gastrointestinal adsorption or to enhance elimination of some drugs

Catharsis

• A. Indications: For stimulation of peristalsis to hasten the elimination of unabsorbed drugs and poisons and the activated charcoal slurry.

• B. Contraindications and Cautions: Do not use mineral oil or other oil-based cathartics. Avoid sodium-based cathartics in patients with hypertension, renal failure, and congestive heart failure and magnesium-based cathartics in those with renal failure.

• C. Technique: Magnesium sulfate 10%, 2–3 mL/kg; or sorbitol 70%, 1–2 mL/kg. Sorbitol is commonly used in prepackaged charcoal slurry products.

Whole Bowel Irrigation

• Whole bowel irrigation utilizes large volumes of balanced polyethylene glycol-electrolyte solution to mechanically cleanse the entire intestinal tract. There is no net gain or loss of systemic fluids or electrolytes.

• Indications: Whole bowel irrigation is particularly effective for massive iron ingestion in which intact tablets are visible on abdominal x-ray. It has also been used for ingestions of sustained-release and enteric-coated tablets as well as drug-filled packets.

• B. Contraindications: Same as for cathartics.• C. Technique: Administer the balanced

polyethylene glycol-electrolyte solution (CoLyte, GoLYTELY) into the stomach via gastric tube at a rate of 1–2 L/h until the rectal effluent is clear

Increased Drug Removal

• Forced Diuresis

• Dialysis (Hemodialysis or Hemoperfusion)

• Repeat-Dose Charcoal

DIAGNOSIS OF POISONING

• Sympathomimetic Syndrome

• Sympatholytic Syndrome

• Cholinergic Syndrome

• Anticholinergic Syndrome

Sympathomimetic Syndrome

• The blood pressure and pulse rate are elevated, though with severe hypertension reflex bradycardia may occur. The temperature is often elevated, pupils are dilated, and the skin is sweaty, though mucous membranes are dry. Patients are usually agitated, anxious, or frankly psychotic.

• Examples: Amphetamines, cocaine, ephedrine and pseudoephedrine, phencyclidine (pupils normal or small), phenylpropanolamine (bradycardia common)

Sympatholytic Syndrome

• The blood pressure and pulse rate are decreased and body temperature is low. The pupils are small or even pinpoint. Peristalsis is usually decreased. Patients are usually obtunded or comatose.

• Examples: Barbiturates, benzodiazepines and other sedative hypnotics, clonidine and related antihypertensives, ethanol, opioids.

Cholinergic Syndrome

• Stimulation of muscarinic receptors causes bradycardia, miosis, sweating, and hyperperistalsis as well as bronchorrhea, wheezing, excessive salivation, and urinary incontinence. Nicotinic receptor stimulation may produce initial hypertension and tachycardia as well as fasciculations and muscle weakness. Patients are usually agitated and anxious.

• Examples: Carbamates, nicotine, organophosphates, physostigmine

Anticholinergic Syndrome

• Tachycardia with mild hypertension is common, and the body temperature is often elevated. Pupils are widely dilated. The skin is flushed, hot and dry. Peristalsis is decreased, and urinary retention is common. Patients may have myoclonic jerking or choreoathetoid movements. Agitated delirium is frequently seen, and severe hyperthermia may occur.

• Examples: Atropine, scopolamine, other naturally occurring and pharmaceutical anticholinergics, amantadine, antihistamines, phenothiazines (hypotension, small pupils), tricyclic antidepressants.